| Stereochemistry | ACHIRAL |
| Molecular Formula | C2H2Cl2O2 |
| Molecular Weight | 128.942 |
| Optical Activity | NONE |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
OC(=O)C(Cl)Cl
InChI
InChIKey=JXTHNDFMNIQAHM-UHFFFAOYSA-N
InChI=1S/C2H2Cl2O2/c3-1(4)2(5)6/h1H,(H,5,6)
| Molecular Formula | C2H2Cl2O2 |
| Molecular Weight | 128.942 |
| Charge | 0 |
| Count |
MOL RATIO
1 MOL RATIO (average) |
| Stereochemistry | ACHIRAL |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Optical Activity | NONE |
Dichloroacetic acid, often abbreviated DCA (dichloroacetate), is an acid analog of acetic acid in which two of the three hydrogen atoms of the methyl group have been replaced by chlorine atoms. The salts and esters of dichloroacetic acid are called dichloroacetates. Salts of DCA are used as drugs since they inhibit the enzyme pyruvate dehydrogenase kinase. Early reports of its activity against brain cancer cells led patients to treat themselves with DCA, which is commercially available in non-pharmaceutical grade. A phase 1 study in 5 patients concluded that DCA was safe, but wasn't designed to establish effectiveness.
DCA was approved for use in Canada in 1989 (as a topical formulation for the treatment of warts and for cauterization and removal of a wide variety of skin and tissue lesions), but was cancelled post market. DCA is a noncompetitive inhibitor of the endoplasmic reticulum enzyme HMG CoA reductase, which catalyzes the rate limiting step in cholesterol biosynthesis. DCA has been researched in adults, children, animals, and cells as a monotherapy as well as in
combination with other therapies for the treatment of severe metabolic disorders including diabetes and hypercholesterolemia, lactic acidosis, certain heart conditions, and cancer. DCA has been prescribed to reduce tumour size and tumour markers, prevent angiogenesis, reduce
cancer related symptoms, manage pain, and aid in palliation.
CNS Activity
Approval Year
PubMed
Patents
Sample Use Guides
Brain Cancer treatment: Oral DCA given twice daily for the 24 week period of the study.
Route of Administration:
Oral
Cells were treated with 25 and 50 mmol/L dichloroacetate
for 24 hours, and cell-cycle profiles were analyzed using
flow cytometry. Dichloroacetate treatment induced changes in the
cell-cycle profiles of all tested glioblastoma cells.
Specifically, after 24 hours of treatment with 25 mmol/L dichloroacetate, there was a slight increase (not significant) in the
cells in G2–M phase in U87 and U251 cells and a 1.2-fold increase
(P < 0.001) in RN1 cells. Significant increase in the mean
percentage of all 3 tested cell lines in G2–M phase was observed
when dichloroacetate dose was increased to 50 mmol/L.
When compared with untreated control (U251, 8.8%; U87,
15.2%; RN1, 14.1%), dichloroacetate treatment increased the
proportion of cells at G2–M phase to 35.5%, 34.7%, and
45.5%, respectively
